All articles tagged with #csf
Specialized brain cells called tanycytes clear tau proteins from cerebrospinal fluid into the bloodstream, helping remove potentially toxic tau from the brain. In Alzheimer's disease, tanycytes are damaged and less tau moves to the blood, correlating with brain tau buildup; this reveals a potential mechanism for disease progression and a new target to boost tau clearance.
New research reveals a skull bone marrow–tumor immune axis in childhood brain cancers: CSF-borne signals educate skull hematopoietic stem and progenitor cells to present tumor antigens via MHC-II, polarizing CD4+ T cells toward regulatory T cells and promoting immunotolerance. Disrupting this axis—by normalizing CSF cytokines, mobilizing skull hematopoiesis, or blocking GM-CSF signaling with mavrilimumab (and even more so when combined with immune checkpoint blockade)—induces tumor regression in mouse models of ZFTA–RELA ependymoma, choroid plexus carcinoma, and group 3 medulloblastoma. The findings identify a skull-tumor immunological interface and suggest targeting local skull hematopoiesis as a potentially less-toxic therapy for aggressive pediatric brain tumors.
Two recent preprints describe proteomic studies that have identified potential biomarkers for early Alzheimer's disease. One study focused on individuals with autosomal dominant Alzheimer's disease (AD) and found 125 proteins in the cerebrospinal fluid (CSF) that distinguished carriers of familial AD mutations from noncarriers, with extracellular matrix protein SMOC1 potentially being an early biomarker. Another study examined plasma proteins in sporadic AD and identified 100 proteins more abundant in AD patients, with eight proteins associated with cognitive decline. These findings suggest that proteomic markers may be specific to CSF or plasma and could aid in early diagnosis and understanding of AD pathology.
Researchers have identified several blood biomarkers that can aid in the diagnosis and monitoring of Alzheimer's disease, including CSF biomarkers such as Aβ42/Aβ40 and p-tau217, as well as plasma biomarkers such as β-amyloid 42/40 and phospho-tau217. These biomarkers have been shown to correlate with amyloid and tau pathology in the brain, and can be used in clinical practice and trials to track disease progression and response to treatment.